Studies on the mechanisms responsible for a variety of abortive infections with oncogenic and "non-oncogenic" adenoviruses are continuing. The oncogenic adenovirus, type 12, abortively infects hamster cells (line BHK21), and in cultures brought to G1 arrest by growth in low serum initiates a cycle of cellular DNA synthesis and mitosis, but ultimately leads to death of most cells, and transformation of a very small minority of the infected population. Under present study are (1) the nature and fate of the cellular DNA synthesized as a result of virus infection, and (2) the nature of the RNA required for initiation of cellular DNA synthesis. Studies on the effect of cyclic AMP have been extended to the productive infection of these cells with the non-oncogenic Ad2, as well as to the endogenous levels of cyclic AMP in adenovirus transformed or infected, and normal hamster cells under various conditions. A second abortive system under study is the restriction to adenovirus replication imposed upon hamster cells when they become transformed by an oncogenic adenovirus. An inhibitor of virus replication can be extracted from these cells, and the purification of this material is currently being pursued. A third abortive system being studied is that in which adenovirus replication is uniquely dependent upon an exogenous supply of arginine. The requirement for arginine in normal cell multiplication is being investigated as part of this problem.